All Publications

  • A refined palate: Bacterial consumption of host glycans in the gut GLYCOBIOLOGY Marcobal, A., Southwick, A. M., Earle, K. A., Sonnenburg, J. L. 2013; 23 (9): 1038-?
  • Complex Interactions Among Diet, Gastrointestinal Transit, and Gut Microbiota in Humanized Mice GASTROENTEROLOGY Kashyap, P. C., Marcobal, A., Ursell, L. K., Larauche, M., Duboc, H., Earle, K. A., Sonnenburg, E. D., Ferreyra, J. A., Higginbottom, S. K., Million, M., Tache, Y., Pasricha, P. J., Knight, R., Farrugia, G., Sonnenburg, J. L. 2013; 144 (5): 967-977


    Diet has major effects on the intestinal microbiota, but the exact mechanisms that alter complex microbial communities have been difficult to elucidate. In addition to the direct influence that diet exerts on microbes, changes in microbiota composition and function can alter host functions such as gastrointestinal (GI) transit time, which in turn can further affect the microbiota.We investigated the relationships among diet, GI motility, and the intestinal microbiota using mice that are germ-free (GF) or humanized (ex-GF mice colonized with human fecal microbiota).Analysis of gut motility revealed that humanized mice fed a standard polysaccharide-rich diet had faster GI transit and increased colonic contractility compared with GF mice. Humanized mice with faster transit due to administration of polyethylene glycol or a nonfermentable cellulose-based diet had similar changes in gut microbiota composition, indicating that diet can modify GI transit, which then affects the composition of the microbial community. However, altered transit in mice fed a diet of fermentable fructooligosaccharide indicates that diet can change gut microbial function, which can affect GI transit.Based on studies in humanized mice, diet can affect GI transit through microbiota-dependent or microbiota-independent pathways, depending on the type of dietary change. The effect of the microbiota on transit largely depends on the amount and type (fermentable vs nonfermentable) of polysaccharides present in the diet. These results have implications for disorders that affect GI transit and gut microbial communities, including irritable bowel syndrome and inflammatory bowel disease.

    View details for DOI 10.1053/j.gastro.2013.01.047

    View details for Web of Science ID 000317813900026

    View details for PubMedID 23380084

  • Initial transference of wild birds to captivity alters stress physiology GENERAL AND COMPARATIVE ENDOCRINOLOGY Dickens, M. J., Earle, K. A., Romero, L. M. 2009; 160 (1): 76-83


    Maintaining wild animals in captivity has long been used for conservation and research. While often suggested that captivity causes chronic stress, impacts on the underlying stress physiology are poorly understood. We used wild-caught chukar (Alectoris chukar) as a model avian species to assess how the initial 10 days of captivity alters the corticosterone (CORT) secretory pathway. In the first few days of captivity, birds lost weight, had lower hematocrit and demonstrated changes in CORT concentrations. Both baseline and restraint-stress-induced CORT concentrations decreased by days 3-5 of captivity and remained significantly lower throughout the 10 days although stress-induced concentrations began to recover by day 9. To delineate potential mechanisms underlying these CORT changes, we evaluated alterations to the hypothalamic-pituitary-adrenal (HPA) axis. Although chukar appear to be resistant to arginine vasotocin's (AVT) effects on CORT release, adrenocorticotropin hormone (ACTH) stimulated CORT release; however, ACTH stimulation did not differ during the 10 days of captivity. In contrast, negative feedback axis sensitivity, as determined by both dexamethasone suppression as well as endogenous negative feedback, decreased by day 5 but was regained by day 9. In addition, the combined stressors of capture and long distance transport eliminated the animals' ability to mount an acute CORT response on the day following the move. Therefore, introduction into captivity appeared to shift the chukar into a temporary state of chronic stress that began to recover within 9days. The duration of these alterations likely varies due to differences in capture techniques, transport distance, and species studied.

    View details for DOI 10.1016/j.ygcen.2008.10.023

    View details for Web of Science ID 000262313200009

    View details for PubMedID 19026651

  • The effect of chronic psychological stress on corticosterone, plasma metabolites, and immune responsiveness in European starlings GENERAL AND COMPARATIVE ENDOCRINOLOGY Cyr, N. E., Earle, K., Tam, C., Romero, L. M. 2007; 154 (1-3): 59-66


    Although increases in glucocorticoid concentrations during acute stress are believed to help animals survive stressful events, chronic changes in glucocorticoid concentrations can alter metabolism and lead to disease. We studied the effect of chronic psychological stress on corticosterone (CORT), corticosterone binding globulin (CBG), glucose, and triglyceride concentrations as well as immune responsiveness to a T-cell mitogen challenge in European starlings, Sturnus vulgaris. To induce chronic stress we used a chronic stress protocol consisting of five stressors (loud radio, cage tapping, cage rolling, human voice, and bag restraint) administered in random order for 30 min for 4 times/day over 18 days. Total CORT decreased throughout the chronic stress period, which parallels a previous study with starlings. CBG capacity did not significantly change with chronic stress, thus free CORT followed the same pattern of attenuation as total CORT during chronic stress. Despite the change in regulation of CORT release, daytime glucose and triglyceride concentrations did not change with chronic stress. In addition, immune responsiveness in chronically stressed and unstressed birds was similar. Our results, together with a previous study using a similar CSP in European starlings, suggest that starlings physiologically dampen the HPA axis during chronic psychological stress to avoid pathology associated with chronically augmented CORT concentrations such as hyperglycemia and impaired immune function.

    View details for DOI 10.1016/j.ygcen.2007.06.016

    View details for Web of Science ID 000249641100008

    View details for PubMedID 17681504

Stanford Medicine Resources: